Ependyma: Normal and pathological. A review of the literature☆

Bruni, J.; Bigio, Marc R. Del; Clattenburg, R. E.

doi:10.1016/0165-0173(85)90016-5

Cited by 163 publications

(89 citation statements)

References 163 publications

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“…The nestin-positive cells seen in this study have the morphological appearance of tanycytes [23][24][25]28 and appear in the proportions described for ependymal cells in vitro: cuboidal, 75%; tanycytes, 19%; and secretory, 6%. 38 An extensive review 26 of hypothalamic tanycytes identifies their role in neuroendrocrine function, suggesting that they act as a bridge between the CSF and the portal venous system, and that they are the only radial glia descendants remaining in adulthood, suggesting a neural progenitor role.…”

Section: Discussionmentioning

confidence: 69%

“…Tanycytes located in the ependyma of the brain have neuroendocrine functions, transport small molecules between the brain and the cerebrospinal fluid (CSF), and have the potential for neurogenesis. 24,27 Their counterparts in the spinal cord are morphologically quite similar, 23 but their specific function in the spinal cord has not been determined. It is thought that they may have a role in transporting or modifying substances moving between the CSF, and the perivascular and extracellular space, 28 and that they may be the reactive cells in the ependyma that respond to injury by proliferating.…”

Section: Discussionmentioning

confidence: 99%

“…Dromard and associates 17 indicated a cluster of nestin-positive cells located in the ventral subependymal region as being a possible neurogenic niche, whereas Hamilton and associates 8 reported that cells with stem cell characteristics may be located in the dorsal pole of the central canal and have a tanycytelike morphology. Rat tanycytes in the ependyma lining the cerebral ventricles and spinal cord have been described in detail, [23][24][25] and although they have little regenerative capacity, they do respond to injury and have a stronger response in the spinal cord than in the brain.…”

Section: Introductionmentioning

confidence: 99%

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Nestin-Positive Ependymal Cells Are Increased in the Human Spinal Cord after Traumatic Central Nervous System Injury

Cawsey

Duflou

Weickert

et al. 2015

Journal of Neurotrauma

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Endogenous neural progenitor cell niches have been identified in adult mammalian brain and spinal cord. Few studies have examined human spinal cord tissue for a neural progenitor cell response in disease or after injury. Here, we have compared cervical spinal cord sections from 14 individuals who died as a result of nontraumatic causes (controls) with 27 who died from injury with evidence of trauma to the central nervous system. Nestin immunoreactivity was used as a marker of neural progenitor cell response. There were significant increases in the percentage of ependymal cells that were nestin positive between controls and trauma cases. When sections from lumbar and thoracic spinal cord were available, nestin positivity was seen at all three spinal levels, suggesting that nestin reactivity is not simply a localized reaction to injury. There was a positive correlation between the percentage of ependymal cells that were nestin positive and post-injury survival time but not for age, postmortem delay, or glial fibrillary acidic protein (GFAP) immunoreactivity. No doublelabelled nestin and GFAP cells were identified in the ependymal, subependymal, or parenchymal regions of the spinal cord. We need to further characterize this subset of ependymal cells to determine their role after injury, whether they are a population of neural progenitor cells with the potential for proliferation, migration, and differentiation for spinal cord repair, or whether they have other roles more in line with hypothalamic tanycytes, which they closely resemble.

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Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nestin-Positive Ependymal Cells Are Increased in the Human Spinal Cord after Traumatic Central Nervous System Injury

Cawsey

Duflou

Weickert

et al. 2015

Journal of Neurotrauma

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“…Neuronal cilia are nonmotile and are thought to function in chemosensation and mechanosensation (28). Ependymal cells lining the cerebral ventricles possess numerous motile cilia and facilitate the circulation of CSF through the ventricles (24,29). In this study, we observed a BBS mouse model phenotype that may be the consequence of aberrant ependymal cell cilia morphology and/or function.…”

Section: Discussionmentioning

confidence: 70%

A knockin mouse model of the Bardet–Biedl syndrome 1 M390R mutation has cilia defects, ventriculomegaly, retinopathy, and obesity

Davis

Swiderski

Rahmouni³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

246

310

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Bardet-Biedl syndrome (BBS) is a genetically heterogeneous disorder that results in retinal degeneration, obesity, cognitive impairment, polydactyly, renal abnormalities, and hypogenitalism. Of the 12 known BBS genes, BBS1 is the most commonly mutated, and a single missense mutation (M390R) accounts for Ϸ80% of BBS1 cases. To gain insight into the function of BBS1, we generated a Bbs1 M390R/M390R knockin mouse model. Mice homozygous for the M390R mutation recapitulated aspects of the human phenotype, including retinal degeneration, male infertility, and obesity. The obese mutant mice were hyperphagic and hyperleptinemic and exhibited reduced locomotor activity but no elevation in mean arterial blood pressure. Morphological evaluation of Bbs1 mutant brain neuroanatomy revealed ventriculomegaly of the lateral and third ventricles, thinning of the cerebral cortex, and reduced volume of the corpus striatum and hippocampus. Similar abnormalities were also observed in the brains of Bbs2 ؊/؊ , Bbs4 ؊/؊ , and Bbs6 ؊/؊ mice, establishing these neuroanatomical defects as a previously undescribed BBS mouse model phenotype. Ultrastructural examination of the ependymal cell cilia that line the enlarged third ventricle of the Bbs1 mutant brains showed that, whereas the 9 ؉ 2 arrangement of axonemal microtubules was intact, elongated cilia and cilia with abnormally swollen distal ends were present. Together with data from transmission electron microscopy analysis of photoreceptor cell connecting cilia, the Bbs1 M390R mutation does not affect axonemal structure, but it may play a role in the regulation of cilia assembly and/or function.B ardet-Biedl syndrome [BBS, Online Mendelian Inheritance in Man (OMIM) 209900] is a genetically heterogeneous autosomal recessive disorder characterized by obesity, retinal degeneration, polydactyly, cognitive impairment, hypogenitalism, and renal abnormalities, as well as susceptibility to hypertension, diabetes mellitus, olfaction deficits, and congenital cardiac defects. Twelve BBS genes (BBS1-12) have been identified to date (1-14). They encode a set of proteins thought to play a role in the structure or function of cilia, basal bodies, and intracellular transport (15, 16). Mutations in BBS1 are the most commonly observed in BBS. A single missense mutation that converts a methionine codon to an arginine codon (M390R) accounts for Ϸ80% of BBS1 mutations and is involved in 25% of all BBS cases (5). The M390R mutation occurs near predicted regions of coiled-coil protein domains and lies within a conserved predicted WD40-like protein motif. These protein motifs are involved in such basic biological processes as signal transduction, RNA synthesis/processing, chromatin assembly, vesicular trafficking, cytoskeletal assembly, cell cycle control, and apoptosis (17).Recently, BBS1, BBS2, BBS4, BBS5, BBS7, BBS8, and BBS9 were shown to form a stable Ϸ450-kDa protein complex called the BBSome in cultured retinal pigment epithelial (RPE) cells and mouse testes. Depletion of some components of the BBSome, ...

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“…Ependymal cells represent an independent type of the glial cells in the frame of the nervous system (Brightman & Palay 1963;Bruni et al 1985;Morest & Silver 2003).…”

Section: Introductionmentioning

confidence: 99%

Method of labelling of individual ependymal areas according to periventricular structures of the rat lateral brain ventricles

Mitro

2014

Biologia

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Ependymal areas were studied in the lateral brain ventricles of the rat central nervous system and were labelled with a code. The presented suggestion using the coding for individual ependymal areas in rat ventricle may solve the significant problem in experimental studies, i.e. how to secure the mutual comparison of the same type of ependymal areas or ependymal cells. The periventricular structures represent a basic and stable part of brain nerve tissue and they are localized most closely to the studied part of the ventricle wall. For this quality they were chosen as reference nerve tissue for the labelling of the ependymal areas and they were used for the creation of the code. The code is composed from letters "Lv" (lateral ventricle) and "E" (ependymal area) followed by the abbreviation of the latin name of the periventricular structure, e.g., the corpus callosum abbreviation is "cc". The code of the ependymal area over the corpus callosum is thus "LvE-cc". The proposed labelling of the ependymal areas may offer several advantages, such as: (i) better characterization of ependymal areas in the future; (ii) preventing the interchange of different types of ependymal areas or ependymal cells; and (iii) avoiding a false interpretation in experiments.

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Ependyma: Normal and pathological. A review of the literature☆

Cited by 163 publications

References 163 publications

Nestin-Positive Ependymal Cells Are Increased in the Human Spinal Cord after Traumatic Central Nervous System Injury

Nestin-Positive Ependymal Cells Are Increased in the Human Spinal Cord after Traumatic Central Nervous System Injury

A knockin mouse model of the Bardet–Biedl syndrome 1 M390R mutation has cilia defects, ventriculomegaly, retinopathy, and obesity

Method of labelling of individual ependymal areas according to periventricular structures of the rat lateral brain ventricles

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